UPMC Montefiore

Traditional residency application review methods are fraught with bias. Literature on how to create and use rubrics to aid in holistic review is lacking. The authors describe their residency program's process of designing and implementing a mission-based rubric to aid in holistic review. After updating the University of Pittsburgh Medical Center internal medicine-pediatrics residency program's mission statement in April 2020, the authors used experiences, attributes, and metrics domains to create a rubric based on the Electronic Residency Application Service application. The rubric included sections on the personal statement, Medical Student Performance Evaluation notable points and curriculum vitae data, additional positives, academic metrics, and red flags, with each section weighted based on alignment with the program's mission and values. The authors, as program leadership, found the rubric to be clear, efficient, and replicable, requiring ~15-20 minutes to read, review, and score each application. The rubric aided in equitable scoring across reviewers, with underrepresented in medicine (URM) applicants scoring similarly to non-URM applicants for the 2020-2021, 2021-2022, and 2022-2023 seasons, and led to reproducible results with an intraclass correlation coefficient of 0.82. The rubric led to an increase in the number of applicants who identify as URM in the initial top 10 rank list each season, as compared to the prior 3 seasons, and the holistic review scores served as a starting point for a final rank list. Larger programs could scale similar holistic review processes by training additional reviewers to use the rubric or implementing it at various stages in the recruitment process. The authors were prompted to consider and improve ways their program could support potential residents. By implementing holistic review, programs can recruit diverse applicant classes that reflect their mission, values, and communities served, while mitigating biases inherent to graduate medical education systems.

The Achilles tendon is the strongest and largest tendon in the human body, composed of the distal confluence of the gastrocnemius and soleus muscles and may also include the plantaris longus tendons. Despite its tremendous strength, it is frequently injured. Soft tissue tumors or tumor-like conditions of Achilles tendon are much less common in comparison to traumatic and infectious/inflammatory lesions. These include giant cell tumor of the tendon sheath, pigmented villonodular synovitis, xanthomas, hematomas, and tophaceous gout. We present a case of a myxochondroid mass arising from the Achilles tendon in a 17-year-old female softball player detected after a minor trauma. According to our knowledge, this is the first case reported in the literature detailing the radiological findings and histopathological diagnosis of a myxochondroid mass arising from a tendon.

Many interventions implemented for multi-visit patients (MVP) have been developed to address patient-centric needs of these individuals and reduce unplanned care for ambulatory-sensitive conditions. More rigorous research is needed to better understand the impact of these interventions on changes in care utilization including unplanned care. To evaluate the impact of the Enhanced Care Program (ECP), a payer-provider collaborative model, on unplanned care use and cost of care. Using propensity methods, a comparison group was constructed using insurer membership files. Comparisons were performed using a difference-in-differences analysis. Patients enrolled in ECP through December 2019 were considered eligible for the study (n = 357). All patients had five or more ED visits in the past year or two or more inpatient hospitalizations in the past year prior to enrollment. ECP is a high-intensity outpatient intervention intended to reduce avoidable unplanned care such as ED visits and inpatient hospital stays through home visits, chronic/acute disease management, and intensive care coordination. The primary outcomes of interest were events per 100 members per year of ED use with return to home, unplanned inpatient and observational status admissions, and unplanned behavioral health inpatient admission, and cost of care per member per month. Overall total unplanned care encounters were significantly reduced with a difference-in-difference of 320 unplanned care encounters per 100 members per year in the intervention group (p < 0.05). The ECP group showed statistically significant decreases in costs of unplanned ED, unplanned observation admission, and unplanned inpatient behavioral medicine costs, but statistically significant increases in overall pharmacy costs and lab costs. Changes in total costs of care for the ECP group were not statistically different than the control group (p = 0.55). ECP showed significant reduction of unplanned care for MVP patients.

Cefepime neurotoxicity is a well-documented though underrecognized cause of encephalopathy. This report describes a case of cefepime-induced Cotard syndrome, a rare delusional syndrome marked by a belief that one is dead.

The incidence of cancer in thyroid nodules carrying germline or somatic phosphatase and tensin homolog (PTEN) mutations is not well-defined. This study characterizes the clinical and histopathologic features of thyroid nodules with preoperatively detected PTEN mutations and their impact on management. Thyroid nodules with PTEN mutations on molecular testing of fine-needle aspiration (FNA) specimens from November 2017 to July 2020 at our institution were included. Demographic and clinicopathologic data were obtained through retrospective chart review. We identified 49 PTEN mutation-positive nodules from 48 patients. Surveillance was pursued for 28 patients and surgery for 20 patients. There were 14 follicular adenomas (FA), 4 oncocytic adenomas, 1 oncocytic hyperplastic nodule, and 1 encapsulated follicular variant papillary thyroid carcinoma (EFVPTC). The EFVPTC had two somatic PTEN mutations, an NRAS mutation, and was a low-risk tumor with capsular but no angiolymphatic invasion. Four patients, all with multiple nodules, had PTEN hamartoma syndrome (PHTS) with germline mutations or a clinical diagnosis of Cowden syndrome (CS); two had surgery finding FAs, and one previously had follicular carcinoma removed. Among surveillance patients, 1/20 had a significant increase in the size of the thyroid nodule and underwent repeat FNA, and no thyroid malignancy was found with a mean of 1.77 years of follow-up (range 1.00-2.78). Thyroid nodules with isolated somatic PTEN mutations are primarily benign and unlikely to grow at a high rate, at least on short-term follow-up. About 8% of patients with PTEN mutations may have PHTS or CS, which should be suspected in younger patients with multiple thyroid nodules.

BackgroundGenes involved in lung development may become dysregulated in adult life and contribute to the pathogenesis of lung diseases. Multiple genes regulate lung development, including Forkhead box protein P1-4 (FoxP1-4).MethodsWe examined the association between variants in the FoxP1-4 genes and lung function using data from a GWAS that included close to 400,000 individuals and 20 million SNPs.ResultsMore than 100 variants in the FoxP1 gene, but none in the FoxP2-4 genes, are associated with lung function. The sentinel variant in the FoxP1 gene associated with FEV1 was rs1499894 (C > T), while the sentinel variant in the FoxP1 gene associated with FVC was rs35480566 (A > G). Those with the T allele instead of the C allele for rs1499894, or the G allele instead of the A allele for rs35480566 had increased FoxP1 mRNA levels in transcriptomic data, higher FEV1 and FVC, and reduced odds of being diagnosed with idiopathic pulmonary fibrosis. Further, knockdown of FoxP1 in lung epithelial cells by RNA interference led to increased mRNA levels for matrix metalloproteinases 1, 2, 3 and pro-inflammatory cytokines IL-6 & IL-8, as well as reduced cell viability after exposure to cigarette smoke—all processes implicated in the pathogenesis of COPD and IPF.ConclusionsOur results suggest that the protein encoded by the FoxP1 gene may protect against the development of COPD and IPF. A causal role for FoxP1 in the pathogenesis of COPD and IPF may warrant further investigation, and FoxP1 may be a novel therapeutic target for these lung disorders.